In the past, acute kidney injury (AKI) used to be called acute renal failure or insufficiency. Among the most common causes of acute renal failure is so-called prerenal azotemia, which occurs when renal perfusion is inadequate or compromised, leading to a transient elevation of serum creatinine level. This can happen as a result of reduced intravascular volume caused by relative dehydration or blood or fluid loss. It also can result from low effective arterial volume even if the patient is otherwise fluid overloaded, such as in the setting of heart failure (cardiorenal) or liver disease (hepartorenal syndrome).

When there is potential fluid loss or low blood pressure, a trial of fluid resuscitation is the conventional approach. Usually, normal saline or other types of osmotically effective fluids such as albumin infusions are administered. If prerenal azotemia is not corrected effectively, the comprised renal perfusion leads to ischemic injury and ultimately acute tubular necrosis (ATN).  When ATN with worsening uremia and electrolyte disarrays persist, dialysis treatment is inevitable and often combined with fluid removal via ultrafiltration. To date, however, no credible study has shown that either intermittent or slow continuous dialysis therapy can improve AKI outcomes. Indeed, most studies have consistently suggested that patient outcome is poorer and mortality is higher when dialysis is initiated.

More recently, AKI has been considered any transient elevation in serum creatinine. There is a tendency to avoid fluid administration for AKI and to start dialysis therapy earlier to remove fluid. Published studies and industry-sponsored lectures have suggested that we should start dialysis earlier and remove more fluid even before creatinine is elevated. Not infrequently, other specialists, particularly intensivists, cardiologists, and cardiothoracic surgeons, want more fluid removed so chest X-rays look drier. Loop diuretics often are ineffective, so dialysis therapy with large amounts of ultrafiltration is desired, no matter how harmful such interventions are to the injured kidneys.

A good nephrologist and astute clinician is the one who resists all these pressures and defends renal perfusion. Although fluid removal may improve pulmonary vascular congestion or ventricular contractility, renal ischemia will likely lead to prerenal azotemia and ATN and prolonged oligoanuric AKI.  The nephrologist should advocate more fluid administration and better renal perfusion, and use dialysis with the least frequency and fluid removal as the last resort in AKI management. If the nephrologist gives into pressure from other specialists to remove fluid, then who else is left to protect the kidney?